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Melatonin slows ALS symptoms in mice

U. PITTSBURGH (US) — Injections of melatonin delayed the onset of symptoms and death in mice with a condition similar to Lou Gehrig’s disease.

The findings—which show that receptors for the hormone are found in the nerve cells—could pave the way for new therapeutic approaches.

Annually about 5,000 people are diagnosed with amyotrophic lateral sclerosis (ALS), a neurodegenerative condition characterized by progressive muscle weakness and eventual death due to the failure of respiratory muscles. But the causes of the condition are not well understood, thwarting development of a cure or even effective treatments.

Melatonin is a naturally occurring hormone that is best known for its role in sleep regulation. After screening more than a thousand FDA-approved drugs several years ago, researchers determined that melatonin is a powerful antioxidant that blocks the release of enzymes that activate apoptosis, or programmed cell death.

“Our experiments show for the first time that a lack of melatonin and melatonin receptor 1, or MT1, is associated with the progression of ALS,” says Robert Friedlander, professor of neurosurgery and neurobiology at the University of Pittsburgh School of Medicine and senior investigation of the study published in Neurobiology of Disease.

“We saw similar results in a Huntington’s disease model in an earlier project, suggesting similar biochemical pathways are disrupted in these challenging neurologic diseases,” Friedlander says.

Hoping to stop neuron death in ALS just as they did in Huntington’s, the research team treated mice bred to have an ALS-like disease with injections of melatonin or with a placebo. Compared to untreated animals, the melatonin group developed symptoms later, survived longer, and had less degeneration of motor neurons in the spinal cord.

“Much more work has to be done to unravel these mechanisms before human trials of melatonin or a drug akin to it can be conducted to determine its usefulness as an ALS treatment,” Friedlander says. “I suspect that a combination of agents that act on these pathways will be needed to make headway with this devastating disease.”

Co-authors of the paper include other scientists from the University of Pittsburgh, Harvard Medical School, Ohio State University, Weifang Medical University; University of Texas Medical School at Houston, VA Pittsburgh Health Care System, Bedford VA Medical System in Boston, and St. Joseph’s Hospital and Medical Center in Phoenix.

The National Institutes of Health, the US Department of Defense, and the Muscular Dystrophy Association funded the research.

Source: University of Pittsburgh

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